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1 al disturbances occur in thiamine-responsive megaloblastic anaemia (TRMA), an autosomal recessive dis
6 recessive disorder characterized by juvenile megaloblastic anaemia, as well as neurological symptoms
7 ecessive disorder with features that include megaloblastic anaemia, mild thrombocytopenia and leucope
9 ins, their morphologically indistinguishable megaloblastic anaemias, and their overlapping neuropsych
11 -vitamin B12 receptor, results in hereditary megaloblastic anemia (MGA1), owing to vitamin B12 malabs
12 lasts from patients with thiamine-responsive megaloblastic anemia (TRMA) syndrome with diabetes and d
13 y of the syndrome called thiamine-responsive megaloblastic anemia (TRMA) with diabetes and deafness.
14 described as a cause of thiamine-responsive megaloblastic anemia (TRMA), an autosomal recessive synd
15 iency disorders, such as thiamine-responsive megaloblastic anemia (TRMA), which is associated with sp
21 inborn error of metabolism, characterized by megaloblastic anemia and/or pancytopenia, severe cerebra
22 data) for risk of deficiency on the basis of megaloblastic anemia as a hematologic indicator in perso
24 paired purine nucleotide metabolism, whereas megaloblastic anemia has been associated with impaired d
25 dies of impaired DNA synthesis and repair in megaloblastic anemia have concerned mainly the decreased
27 wed not only as a nutrient needed to prevent megaloblastic anemia in pregnancy but also as a vitamin
28 sm, the degree of uracil misincorporation in megaloblastic anemia is sufficient to increase the stead
29 amage, accounting for the pathophysiology of megaloblastic anemia observed in vitamin B12 and folate
30 Cubulin mutations cause a hereditary form of megaloblastic anemia secondary to vitamin B(12) deficien
33 isincorporated into the DNA of patients with megaloblastic anemia to levels detectable by nonradioact
35 blastic anemia (diabetes mellitus, deafness, megaloblastic anemia) lacking functional Slc19a2 has bee
37 f folate or vitamin B(12) (cobalamin) causes megaloblastic anemia, a disease characterized by pancyto
38 Mutations in THTR-1 cause thiamin-responsive megaloblastic anemia, a tissue-specific disease associat
41 itions (SF3B1-mutant and SF3B1-wildtype MDS, megaloblastic anemia, and iron deficiency anemia), Haemo
44 ary levels of the vitamin folate can lead to megaloblastic anemia, birth defects, impaired cognitive
45 essive disorder defined by the occurrence of megaloblastic anemia, diabetes mellitus, and sensorineur
46 utosomal recessive syndrome characterized by megaloblastic anemia, diabetes, and sensorineural deafne
47 while prevalent in both iron deficiency and megaloblastic anemia, hyperlobulated neutrophils are lar
48 been appreciated for decades in relation to megaloblastic anemia, it has been recently proposed that
50 ral tube defects, homocysteine imbalance and megaloblastic anemia, often associated with cobalamin de
51 However, in patients with thiamin-responsive megaloblastic anemia, plasma thiamin levels are within n
52 and symptoms of vitamin B12 deficiency, e.g. megaloblastic anemia, precise evaluation and treatment i
53 parents had diabetes mellitus, deafness, or megaloblastic anemia, which raised the possibility that
54 linical vitamin B12 deficiency can result in megaloblastic anemia, which results from the inhibition
55 result in negative health outcomes including megaloblastic anemia, with additional neurocognitive imp
63 normal erythropoiesis is a common feature of megaloblastic anemias, congenital dyserythropoietic anem
64 utcomes (specifically acute pain episodes or megaloblastic changes) when individuals were supplemente
65 nemia with abnormal erythroid maturation and megaloblastic changes, as well as profound defects in ly
70 um-free liquid culture into large numbers of megaloblastic nucleated erythroblasts resembling yolk sa